Localisation by in situ hybridisation of S100A4 (p9Ka) mRNA in primary human breast tumour specimens

Citation
Ll. Nikitenko et al., Localisation by in situ hybridisation of S100A4 (p9Ka) mRNA in primary human breast tumour specimens, INT J CANC, 86(2), 2000, pp. 219-228
Citations number
26
Categorie Soggetti
Onconogenesis & Cancer Research
Journal title
INTERNATIONAL JOURNAL OF CANCER
ISSN journal
00207136 → ACNP
Volume
86
Issue
2
Year of publication
2000
Pages
219 - 228
Database
ISI
SICI code
0020-7136(20000415)86:2<219:LBISHO>2.0.ZU;2-1
Abstract
Rodent S100A4 (p9Ka) induces a metastatic phenotype in benign rat mammary t umour cells and cooperates with the neu oncogene to produce metastatic tumo urs in a transgenic mouse model system. Human S100A4 possesses similar meta stasis-inducing properties. S100A4 mRNA is now sought in human breast tumou r-derived cell lines and tumour specimens. S100A4 mRNA is present in some c ell lines derived from malignant breast cancers, but is not detectable in c ells derived from benign breast tumours, In human tumour specimens, using i n situ hybridisation, the mRNA for S100A4 is localised to the epithelial ce lls of carcinoma specimens, and in some normal breast specimens, to a strom al region surrounding the epithelial ducts, In carcinoma specimens, S100A4 mRNA is also found in the stromal region surrounding islands of cancer cell s. For both the epithelial and stromal components, S100A4 mRNA is present a t a higher level in carcinomas relative to benign breast tumour specimens. In general, there is a concordance between the S100A4 mRNA signal from the epithelial and stromal elements of the same carcinoma specimens. Using Nort hern blotting techniques, these results have been extended to a panel of 13 7 benign and malignant breast tumour specimens. The results show that S100A 4 mRNA occurs in the more-malignant, rather than in the more-benign tumour specimens. Int. J, Cancer 86: 219-228, 2000. (C) 2000 Wiley-Liss, Inc.